Aberrant functioning of proteins within stress response pathways (e.g. p53, NF-B, heat shock response) are prominent features in many cancer types. Such alterations have been associated with poor response of tumors to conventional antitumor treatments. This is true for such cancers as non-small cell lung cancer, hepatocellular carcinoma, advanced prostate cancer, renal cell carcinoma and glioblastoma multiforme. Targeted therapies against these alterations may restore tumor response to treatment and, thus, improve clinical outcome. Multifunctional agents, such as the Curaxin to be studied in the context of this contract, have the potential to be more effective than drugs that target single pathways since they decrease the likelihood of tumors finding ways to circumvent their effects unlike single function agents where one mutation or inactivation of a component of the targeted pathway would make tumors less sensitive to treatment.